Ganong's Review of Medical Physiology, 23rd Edition

CHAPTER 38Renal Function & Micturition 647

HYDROSTATIC & OSMOTIC PRESSURE

The pressure in the glomerular capillaries is higher than that
in other capillary beds because the afferent arterioles are short,
straight branches of the interlobular arteries. Furthermore, the
vessels “downstream” from the glomeruli, the efferent arteri-
oles, have a relatively high resistance. The capillary hydrostatic
pressure is opposed by the hydrostatic pressure in Bowman’s
capsule. It is also opposed by the oncotic pressure gradient
across the glomerular capillaries (πGC – πT). πT is normally
negligible, and the gradient is essentially equal to the oncotic
pressure of the plasma proteins.
The actual pressures in one strain of rats are shown in Figure
38–6. The net filtration pressure (PUF) is 15 mm Hg at the
afferent end of the glomerular capillaries, but it falls to zero—
that is, filtration equilibrium is reached—proximal to the effer-
ent end of the glomerular capillaries. This is because fluid
leaves the plasma and the oncotic pressure rises as blood passes
through the glomerular capillaries. The calculated change in
Δπ along an idealized glomerular capillary is also shown in
Figure 38–6. It is apparent that portions of the glomerular cap-
illaries do not normally contribute to the formation of the glo-
merular ultrafiltrate; that is, exchange across the glomerular
capillaries is flow-limited rather than diffusion-limited. It is
also apparent that a decrease in the rate of rise of the Δ curve
produced by an increase in renal plasma flow would increase
filtration because it would increase the distance along the capil-
lary in which filtration was taking place.
There is considerable species variation in whether filtration
equilibrium is reached, and some uncertainties are inherent in

the measurement of Kf. It is uncertain whether filtration equi-

librium is reached in humans.

CHANGES IN GFR

Variations in the factors discussed in the preceding para-

graphs and listed in Table 38–4 have predictable effects on the

GFR. Changes in renal vascular resistance as a result of auto-

regulation tend to stabilize filtration pressure, but when the

mean systemic arterial pressure drops below the autoregulato-

ry range (Figure 38–4), GFR drops sharply. The GFR tends to

be maintained when efferent arteriolar constriction is greater

than afferent constriction, but either type of constriction de-

creases blood flow to the tubules.

FILTRATION FRACTION

The ratio of the GFR to the RPF, the filtration fraction, is nor-

mally 0.16 to 0.20. The GFR varies less than the RPF. When

there is a fall in systemic blood pressure, the GFR falls less than

the RPF because of efferent arteriolar constriction, and conse-

quently the filtration fraction rises.

TUBULAR FUNCTION

GENERAL CONSIDERATIONS

The amount of any substance (X) that is filtered is the product

of the GFR and the plasma level of the substance (ClnPX). The

tubular cells may add more of the substance to the filtrate (tu-

bular secretion), may remove some or all of the substance

from the filtrate (tubular reabsorption), or may do both. The

amount of the substance excreted per unit of time (UXV

• )

FIGURE 38–6 Hydrostatic pressure (PGC) and osmotic
pressure (πGC) in a glomerular capillary in the rat. PT, pressure in
Bowman’s capsule; PUF, net filtration pressure. πT is normally negligi-
ble, so Δπ = πGC. ΔP = PGC – PT. (Reproduced with permission from Mercer PF,
Maddox DA, Brenner BM: Current concepts of sodium chloride and water transport
by the mammalian nephron. West J Med 1974;120:33.)

(mm Hg)

Afferent end Efferent end

45

10

20

15

45

10

35

0

PUF = PGC− PT− πGC

PGC

PT

πGC

PUF

Dimensionless distance along

idealized glomerular capillary

Pressure (mm Hg)

60

40

20

0

01

ΔP

Δπ

TABLE 38–4 Factors affecting the GFR.

Changes in renal blood flow

Changes in glomerular capillary hydrostatic pressure

Changes in systemic blood pressure

Afferent or efferent arteriolar constriction

Changes in hydrostatic pressure in Bowman’s capsule

Ureteral obstruction

Edema of kidney inside tight renal capsule

Changes in concentration of plasma proteins:

dehydration, hypoproteinemia, etc (minor factors)

Changes in Kf

Changes in glomerular capillary permeability

Changes in effective filtration surface area